1. Field of the Invention
The present invention relates to devices and related methods for improving the function of heart valves, and more particularly to devices and related methods that passively assist in the apposition of heart valve leaflets to improve valve function of poorly functioning valves.
2. Description of the Related Art
Heart failure is a condition whereby the left ventricle becomes enlarged and dilated as a result of numerous etiologies. Initial causes of heart failure include chronic hypertension, myocardial infarction, mitral valve incompetency, and other dilated cardiomyopathies. With each of these conditions, the heart is forced to overexert itself in order to provide the cardiac output demanded from the body during its various demand states. The result is an enlarged left ventricle.
A dilated heart, and particularly a dilated left ventricle, can significantly increase the tension and/or stress in the heart wall both during diastolic filling and systolic contraction, which contributes to ongoing dilatation of the chamber. Prior treatments for heart failure include pharmacological treatments, assist devices such as pumps, and surgical treatments such as heart transplant, dynamic cardiomyoplasty, and the Batista partial left ventriculectomy. These prior treatments are described briefly in U.S. Pat. No. 5,961,440 to Schweich, Jr. et al., issued Oct. 5, 1999 and entitled “Heart Wall Tension Reduction Apparatus and Method,” the complete disclosure of which is incorporated by reference herein.
A more recent concept for treating heart failure applies one or more splints onto the heart, and particulary the left ventricle, to reduce the myocardial muscular stresses encountered during pumping. Many examples of such approaches are disclosed in the incorporated U.S. Pat. No. 5,961,440. One example includes one or more transventricular splints placed across the left ventricle. Each splint may include a tension member extending across the ventricle and anchors disposed on opposite ends of the tension member and placed on the external surface of the heart.
Mitral valve incompetency or mitral valve regurgitation is a common comorbidity of congestive heart failure. As the dilation of the ventricle proceeds, valve function may worsen. The resultant volume overload condition, in turn, increases ventricular wall stress thereby advancing the dilation process, which may further worsen valve dysfunction.
In heart failure, the size of the valve annulus (particularly the mitral valve annulus) increases while the area of the leaflets of the valve remains constant. This may lead to an area of less coaptation of the valve leaflets, and, as a result, eventually to valve leakage. Moreover, in normal hearts, the annular size contracts during systole, aiding in valve coaptation. In heart failure, there is poor ventricular function and elevated wall stress. These effects tend to reduce annular contraction and distort annular size, often exacerbating mitral valve regurgitation. In addition, as the chamber dilates, the papillary muscles (to which the leaflets are connected via the chordae tendonae) may move radially outward and downward relative to the valve, and relative to their normal positions. During this movement of the papillary muscles, however, the various chordae lengths remain substantially constant, which limits the full closure ability of the leaflets by exerting tension prematurely on the leaflets. This condition is commonly referred to as “chordal tethering.” The combination of annular changes and papillary changes results in a poorly functioning valve.
It has been observed that for at least certain placements, or orientations, of the one or more transventricular splints in humans, a pre-existing mitral valve incompetency can be exacerbated by the presence and impact of the tightened splints. The splints and the local deformation they impart may further alter the positions of the papillary muscles in such a way that the chordae do not allow as complete of a closure of the mitral valve, or that rotation of portions of the ventricular wall (to which additional chordae may be attached) may “tighten” one valve leaflet and “loosen” the other. In this manner, the leaflets may not close at the same level relative to the annulus, causing increased retrograde leakage through the valve.
Even in instances where the placement of splints does not contribute to further mitral valve leakage, it may be desirable to provide a therapy which could also correct the valve incompetency. A heart with even a small amount of regurgitation may benefit from not only the stress reducing functions of the ventricular splints as described above, but also from the elimination of the regurgitation, which will further off-load the pumping requirements of the myocardium.
While currently available methods of mitral valve repair or replacement are possible to employ in conjunction with ventricular splinting, they typically require opening the heart to gain direct access to the valve and its annulus. This type of access necessitates the use of cardiopulmonary bypass, which can introduce additional complications to the surgical procedure. Since the implantation of the splints themselves do not require the patient to be on cardiopulmonary bypass, it would be advantageous to devise a technique which could improve the mitral valve without the need for cardiopulmonary bypass. The ability to improve the mitral valve function without the need for cardiopulmonary bypass would be an advantage, both in conjunction with ventricular splinting, and also as a stand-alone therapy.